Glaucoma

Glaucoma

 The term glaucoma refers to a group of

diseases that have in common :
• A characteristic optic neuropathy
• Associated visual field loss
• Intraocular pressure is usually a key
modifying factor .
 The intraocular pressure (IOP)

• The accepted range of IOP in the general population

is 10-21 mmHg.
• Normal physiological variations in IOP (1-2 mmHg),
varies with :
• Respiration .
• BP, heartbeats .
• Time of day (maximum in the morning).
• IOP measured by:

-Indentation tonometry:
Schiotz tonometry .

-Applanation tonometry:
Goldmann tonometry
• Eye ball can be considered as a closed
system with relatively constant contents,
except the aqueous humor.

• The continuous turnover of aqueous is the

main determinant of IOP.
 Three factors determine the IOP

• The rate of aqueous humor production by the

ciliary body .
• Resistance to the aqueous outflow across the
trabecular meshwork – Schlemm’s canal
system .
• The level of episcleral venous pressure .
• Aqueous Pathway:
 Aqueous is produced from ciliary
processes into the posterior chamber,
passes through the pupil into the anterior
chamber and leave the eye through:

 Angle of anterior chamber ( 90%) the

aqueous passes across trabecular
meshwork into canal of schlemm, and
then drained by the episcleral veins.

 Uveoscleral route (10%) the aqueous

passes across the ciliary body into the
suprachoroidal spaces and is drained by
the venous circulation
• Angle of the anterior
chamber :

 The angle between

the posterior surface
of the cornea and the
anterior surface of
the iris.
• At the angle there is a circumferential porous
meshwork about 1 mm in width called Trabecular
meshwork , through which aqueous drained from the
anterior chamber to canal of Schlemm
• The configuration of the angle indicate the
pathogenesis of glaucoma.
• Contact between the
peripheral iris and the
cornea signifies a
closed angle .

• while wide
separation between
the two indicate open
angle .
 Gonioscopy:
 Examination of the
angle of the anterior
chamber performed by
goniolenses
 Optic disc:
• Anterior end of the optic nerve, about 1.5
mm in diameter. Lies about 3mm from the
fovea. All retinal layers except the nerve
fiber layer stop at the margin of the optic
disc. The nerve fiber layer pass through the
lamina cribrosa a sieve like structure, bridge
the posterior scleral foramen.

• Optic cup; central depression in the optic

disc not occupied by neural tissue.

• Cup/Disc ratio in most normal eyes is 0.3 or

less, asymmetry of 0.2 or more is suspicion.
 Visual Field
 Classification of glaucoma:
• Open angle glaucoma
– Primary open angle glaucoma
– Secondary open angle glaucoma

• Closed angle glaucoma

– Primary closed angle glaucoma
– Secondary closed angle glaucoma

• Congenital glaucoma
Buphthalmus
• Primary glaucomas are not associated with ocular or systemic

disorders that cause increase resistance to aqueous outflow.

• Primary glaucomas usually affect both eyes and may be

inherited.

• Secondary glaucomas are associated with ocular or systemic

disorders that are responsible for increase resistance to

aqueous outflow.

• Secondary glaucomas are usually unilateral and not inherited.

 Primary Open Angle Glaucoma
(POAG)

• Definition : is generally bilateral disease

(although not nessessarly a symmetrical disease )
of adult onset .
 characterized by :
o An IOP > 21 mmHg at some stage .
o Glaucomatous optic nerve damage .
o An open anterior chamber angle .
o Characteristic visual field loss as the damage
progress .
• Increase IOP caused by increase resistant to
aqueous outflow due to thickening of the
trabecular meshwork lamellae, with reduce
in the pores size.
 Theories of glaucomatous damage

Direct damage by pressure Capillary occlusion

Interference with
axoplasmic flow
 Risk factors

• 1- Age
• 2- Race: more common and a more
severe in Blacks .
• 3- Family history and inheritance.
• 4- Myopia: increased incidence of POAG.
• 5- D.M and vascular disease .
 Diagnosis
History
1) Visual symptom will usually be absent , unless damage is advanced .
2) Previous ophthalmic history (Refractive status and causes of secondary
glaucoma )
3) F.H
4) PMH
5) Current medication and allergies .
Examination
1) V.A
2) Pupil
3) SLE
4) Tonometry noting the time of the day
5) Gonioscopy
6) Optic disc examination
7) Perimetry
8) Optic disc or peripapillary RNFL imaging .
 IOP > 21mmHg is
suspicious .
Optic nerve head damage : Increase
in cup/disc ratio.

 Most normal eyes have cup/disc of

0.3 or less

 Increase in cup/disc ratio or

asymmetry between two eyes of 0.2
or more is suspicion.
 Visual field defects :
• Paracentral scotoma .
• arcuate scotoma .
• peripheral field loss with
nasal step
• generalized visual loss,
leaving small central vision
which is lost at the end
• Open angle
assessed by
gonioscopy
 IOP > 21 mmHg Open angle of normal appearance

Glaucomatous disc damage Visual field loss

Management:
 The aim of management is to reduced IOP to the target
pressure (safe pressure) at which no further damage occurs.

 Continuous follow up with checking IOP, examination of the

optic disc and assessment of the visual field is essential.

 Initially primary open angle glaucoma is treated medically with

topical eye-drops, but if IOP is not reduced to the target
pressure then laser therapy or surgery has to be considered
 Treatment:

 Medical:

A-Beta adrenergic blocking drugs .

Mode of action: decrease the aqueous production e.g. Timolol 0.5% eye
drops

B-Topical carbonic anhydrase inhibitors;

Mode of action: decrease the aqueous production e.g. Dorzolmide2% eye

drops

C- Cholinergic drug

Mode of action: increase the aqueous outflow e.g. Pilocarpine 2% eye drops
D- Sympathomimetics drugs;

Mode of action: decrease the aqueous production and

increase uveoscleral aqueous outflow e.g. Brimonidine
0.2% eye drops

E- Prostaglandin derivatives

Mode of action: increase uveoscleral aqueous outflow e.g.

Latanoprost eye drops
2- Laser Trabeculoplasty is a procedure by which the
application of discrete burns to the trabeculum
meshwork enhance aqueous outflow and lower IOP.
3- Surgical : Trabeculectomy (creating a fistula
between the anterior chamber and sub-
Tenon space to by pass the trabecular
meshwork.
 Secondary Open Angle Glaucoma

• Angle is open, but the trabecular meshwork blocked

by:
o Blood (hyphaema) following trauma
o Inflammatory cells(iritis)
o Pigment from the post pigment epithelium of the
iris(pigment dispersion syndrome)
o Deposition of amyloid- like substance
(pseudoexfoliative syndrome)
o Drug induced (steroid induced glaucoma)
• Ocular hypertension;
 IOP>21 without optic disc cupping and visual field
defect.
 7% of the general population above 40 have IOP>21
only 1% of them have glaucoma.

• Normal tension glaucoma;

 patients with IOP= or <21mmHg with optic disc
cupping and visual field defect.
 Primary angle closure glaucoma
(PACG)

 Is a condition in which elevation of

IOP occurs as a result of obstruction
of the aqueous drainage by closure
of the angle with the peripheral iris.
 Anatomical predisposing factors

1- Relative anterior location of

iris-lens diaphragm.
2- Shallow anterior chamber
(AC) due to short axial length
of the eye ( e.g.
hypermetropia).
3- Narrow entrance to anterior
chamber angle.
 Mechanism of angle closure
In most cases PCAG is initiated by;
a- Pupillary Block : which is increase resistance
to aqueous passage between posterior and
anterior chamber by the iris lens contact .

b- Iris bombe : increase pressure in the posterior

chamber, the peripheral iris will bow forward

c- Irido-corneal contact : obstructing the angle .

 If this peripheral irido-
corneal contact persist
for few days then
permanent peripheral
anterior synachae (PAS)
occurs
 Presentation

 Average age of is about 60 years and above

 More common in females

 Frequently bilateral, although presentation is

asymmetrical
 Classification

• 1. Latent

• 2. Subacute

• 3. Acute

• 4. Chronic

• 5. Absolute
 Subacute ( Intermittent) Angle
Closure Glaucoma

• A transient attack of sudden subtotal

closure of the angle results in rapid
increase in IOP, followed by spontaneous
reopening of the angle with the IOP
returns to normal.
 Symptoms

 The attack may be precipitated by physiological mydriasis

(dilation of the pupil) e.g. watching T.V. in dark room

 Sudden onset of

1-Blurring of vision

2-Halloes around light due to corneal edema

3- Sometimes eye-ache or headache

 The attack may last for 1-2 hours and usually broken by
miosis (constriction of the pupil) e.g. exposure to bright light.
 Signs

 During the attack

o Corneal edema

o Shallow anterior chamber

o Elevated IOP

 Between the attacks

o The eye looks normal apart from narrow angle

 Treatment
 Laser iridotomy to create
an opening between the
posterior chamber and
anterior chamber and
bypass the pupillary block

 Both eyes must be treated

with Laser iridotomies
 Acute Angle Closure Glaucoma

 Sudden total closure of the angle with rapid

high increase in IOP.
 Clinical features
 Symptoms  Signs
• Onset : Sudden • Cicum-corneal congestion
• Periocular pain and headache • Corneal edema
• Bluring of vision • Shallow anterior chamber
• Halloes around light due to
• Mid-dilated ,fixed pupil
corneal edema
• IOP elevated
• Redness of the eye
• Sometimes nausea and
vomiting
 Treatment
• Admission to the hospital
• Medical treatment :
 Systemic Carbonic anhydrase inhibitors, initially
Acetazolamide 500mg i.v. followed by 250 mg orally qds.
 Topical 2% pilocarpine qds.
 Topical 0.5% timolol bds.
 If IOP still high after one hour then hyper osmotic agent is
given
 20% mannitol 1-2 gm/kg i.v. over 45 minutes
• After reducing IOP medically treatment is essentially by laser
iridotomy in early cases without established PAS (to create an
opening between the posterior chamber and anterior chamber
and by pass the pupillary block).

• While in late cases with PAS, treatment is with surgical

trabeculotomy to create an opening between the anterior
chamber and sub-conjunctival space and by pass the PAS.

• The other eye must be prophylactically treated with laser

iridotomy.
If urgent management is not given, there
will irreversible damage to the optic nerve
with permanent blindness
 Secondary Closed Angle Glaucoma

• 1- Lens-related glaucoma
• 2- Neovascular glaucoma
• 3- Inflammatory glaucoma
• 4- Intra ocular tumor may push iris lens
diaphragm forward and closing the angle
 1-Lens-related glaucoma:

• a- Phacolytic glaucoma.

• b- Phacomorphic (Intumescent) glaucoma:

• b- Phaco anaphylactic glaucoma:

a- Phacolytic glaucoma
b- Phacomorphic (Intumescent)
glaucoma
 2- Neovascular glaucoma
 Caused by rubeosis iridis associated with chronic, diffuse
retinal ischaemia .

 Causes
1. Central retinal vein occlusion. (commonest cause)
2. Diabetes mellitus (proliferative diabetic retinopathy).
3. Miscellaneous
 Carotid obstructive disease.
 Central retinal artery occlusion.
 Intraocular tumours.
 Long standing retinal detachment.
 Chronic intraocular inflammation.
Inflammatory glaucoma
 Congenital Glaucoma
• Affect 1:10,000 births
o True congenital glaucoma: represents (40%) of all
congenital glaucoma
o 2- Infantile glaucoma: represents (55%) of congenital
glaucomas,
o Juvenile glaucoma: represents (5%) of congenital
glaucomas,
• 75% bilateral
• 65% male
 Clinical features

• Corneal haze.
• Buphthalmos.
• Breaks in descement
membrane. (Haab striae)
• Optic cupping
 Diagnosis

• Corneal diameter
• IOP
• C/D ratio
 Treatment
• Surgical

 Goinotomy .

 Trabeculectomy .